Abstract
Background: Sciatic neuropathy associated with acetabular fractures
can result in disabling long-term symptoms. The purpose of this retrospective
study was to evaluate the effect of sciatic nerve release on sciatic
neuropathy associated with acetabular fractures and reconstructive acetabular
surgery.
Methods: Between 2000 and 2004, ten patients with sciatic neuropathy
associated with an acetabular fracture were treated with release of the
sciatic nerve from scar tissue and heterotopic bone. Additional surgical
procedures included open reduction and internal fixation of the acetabulum
(five patients), removal of hardware and total hip arthroplasty (three
patients), and removal of hardware alone (one patient). The average age of the
patients was forty-three years. All patients were followed with serial
examinations and assessments for a minimum of one year (average, twenty-six
months).
Results: All patients had partial to complete relief of radicular
pain, of diminished sensation, and of paresthesias after the nerve release.
Four of seven patients with motor loss and two of five patients with a
footdrop demonstrated improvement in function after the nerve release. No
patient had evidence of worsening on neurologic examination after the
release.
Conclusions: Sciatic nerve release during reconstructive acetabular
surgery can decrease the sensory symptoms of preoperative sciatic neuropathy
associated with a previous acetabular fracture. Motor symptoms, however, are
less likely to resolve following nerve release.
Level of Evidence: Therapeutic Level IV. See Instructions
to Authors for a complete description of levels of evidence.
The prevalence of sciatic nerve injury following acetabular trauma and
acetabular surgery has been reported to be as high as
30%1-3.
This injury can result in a broad range of clinical symptoms: posterior thigh
pain at the level of the sciatic notch, radicular pain along the sciatic nerve
distribution with motion of the hip and knee, or weakness of muscles
innervated by the sciatic
nerve1,4,5.
The peroneal division of the sciatic nerve is usually affected, with resultant
weakness of the tibialis anterior, extensor hallucis longus, peroneus longus,
and peroneus
brevis6,7.
These symptoms have been mistakenly interpreted as originating from the spine
and have resulted in inappropriate lumbar
decompression8,9.
Several factors associated with the initial acetabular injury and surgical
intervention can result in sciatic neuropathy. The injury, especially when
associated with a posterior hip dislocation, may result in blunt contusion,
laceration, or stretch neurapraxia of the sciatic
nerve1-6,10.
An associated head injury may result in heterotopic ossification, which can
encase and tether the sciatic nerve, restricting its
excursion10-12.
Certain extensile surgical exposures, such as the iliofemoral approach, are
associated with a higher prevalence of heterotopic
ossification13,14.
Failure to provide prophylaxis against heterotopic ossification with
postoperative radiation and/or indomethacin can result in a higher rate of
nerve
entrapment14-17.
Iatrogenic injury can result from placement of posterior retractors with the
hip in flexion, malreduction of the fracture, or poor placement of
hardware1,5,18,19.
Postoperatively, a developing hematoma may progressively compress the nerve,
resulting in
paralysis20,21.
Months to years after surgery, capsular and muscular scarring and hardware
debris or migration can irritate the sciatic nerve and present as a delayed
neuropathy8,9,11,22-25.
The purpose of this retrospective study was to determine if surgical
release of the sciatic nerve from scar tissue, heterotopic bone, and impinging
implants is successful for the treatment of sciatic neuropathy after
acetabular fractures.
Between 2000 and 2004, ten patients with a sciatic nerve injury following
an acetabular fracture were treated by the senior author (D.L.H.) with sciatic
nerve release from scar tissue and heterotopic bone (see Appendix).
Institutional review board approval was obtained for this study. All patients
were followed at regular intervals by the senior author. The average age of
the patients was 42.7 years (range, fifteen to seventy-six years). There were
eight male and two female patients. The average duration of neurologic
symptoms prior to the nerve release was 6.5 months (range, one day to
twenty-two months). The duration of follow-up after the release was twenty-six
months (range, twelve to forty-two months).
In three patients (Cases 2, 3, and 4; see Appendix), the sciatic nerve
deficit was a result of the original injury and was documented prior to open
reduction and internal fixation of the acetabulum. All three of these patients
had pain along the sciatic nerve distribution, and two had a footdrop. In four
patients (Cases 5, 6, 7, and 9), the sciatic nerve injury was first noted
following open reduction and internal fixation of an acetabular fracture. All
of these four patients had pain in the sciatic nerve distribution; in
addition, one had weakness of muscles innervated by the peroneal division
(grade 3 [of 5] weakness of the extensor hallucis longus). In two patients
(Cases 1 and 8), symptoms presented in a delayed manner, weeks after the
acetabular fracture was sustained but prior to open reduction and internal
fixation. These two patients presented for surgical treatment of the
acetabular fracture and sciatic nerve release at five weeks and three months
after the injury, respectively. The first patient had diminished sensation to
light touch in the sciatic nerve distribution and a footdrop. The second
patient had paresthesias in the distribution of the sciatic nerve and severe
weakness of muscles innervated by the peroneal division (grade-1 weakness of
the extensor hallucis longus). In the remaining patient (Case 10), it was
unclear if the nerve injury was posttraumatic or postoperative. This patient
presented with diminished sensation to light touch in the sciatic nerve
distribution and a footdrop.
In addition to sciatic nerve release, five patients underwent open
reduction and internal fixation of the acetabulum, three patients underwent
removal of hardware and a total hip arthroplasty, and one patient underwent
removal of hardware alone. Preoperative diagnoses included an acute acetabular
fracture requiring open reduction and internal fixation in three patients; a
case in which the nerve injury was not diagnosed until five weeks after the
patient sustained the acetabular fracture (the patient presented to us late);
acetabular malunion in three patients, two of whom also had posttraumatic
arthritis; acetabular nonunion and posttraumatic arthritis in one patient;
impinging hardware with extensive heterotopic ossification after acetabular
open reduction and internal fixation in one patient; and extensive heterotopic
ossification after acetabular open reduction and internal fixation in one
patient. A Kocher-Langenbeck surgical approach was used in eight patients; a
triradiate approach, in one patient; and a combined Kocher-Langenbeck and
ilioinguinal approach, in one patient.
The types of acetabular fractures included posterior column/posterior wall
(one), posterior wall (two), transverse (one), T-type (one), both-column
(two), transverse-posterior wall (two), and anterior column/posterior
hemitransverse (one). The mechanisms of the original injury included a fall
(two patients), a motor-vehicle accident (two), a motorcycle accident (one), a
pedestrian struck by a motor vehicle (three), a tractor accident (one), and a
snowboarding accident (one). Five patients had undergone one prior open
reduction and internal fixation of the acetabulum. No patient had an
associated pelvic ring fracture.
Eight patients had electromyography before the sciatic nerve release, and
four of them had findings suggestive of sciatic neuropathy. One of them
demonstrated neuropathy involving the peroneal division of the sciatic nerve,
one demonstrated neuropathy of the tibial division of the sciatic nerve, and
two demonstrated denervation of both divisions of the sciatic nerve. The
remaining electromyographic studies were nondiagnostic. Preoperative computed
tomography was performed for six patients to delineate the acetabular fracture
pattern. One computed tomography scan demonstrated heterotopic ossification
under the abductors, one demonstrated an acetabular nonunion, and one
demonstrated degenerative arthritis of the hip joint. Eight patients had
preoperative magnetic resonance imaging, and four of these scans demonstrated
abnormal findings related to the sciatic nerve: two demonstrated heterotopic
bone encasing the sciatic nerve, one demonstrated scarring around the sciatic
nerve, and one demonstrated an intra-articular screw touching the sciatic
nerve.
Surgical Technique
The Kocher-Langenbeck approach was used to gain access to the sciatic nerve
in all patients. The procedure was performed with use of intraoperative
spontaneous electromyography and/or intraoperative somatosensory evoked
potential
monitoring2,26,27.
A skin incision was made extending from 5 cm distal to the posterior superior
iliac spine to the greater trochanter and then along the femoral shaft
distally. Subcutaneous tissue and then the iliotibial band and the fascia over
the gluteus maximus were divided in line with the skin incision. The
trochanteric bursa was carefully dissected off the external rotators. In most
cases, the sciatic nerve was identified distally by locating the tendon of the
quadratus femoris and following this posteriorly until fibers of the sciatic
nerve were identified. A combination of microdissecting scissors and
osteotomes was used to free the sciatic nerve from scar tissue and encasing
heterotopic bone. All heterotopic bone entrapping the nerve was removed. This
procedure requires careful dissection and takes a considerable amount of time
to avoid further injury to the sciatic nerve. The nerve decompression extended
from below the gluteus maximus insertion on the femur to the greater sciatic
notch. Decompression was performed until the nerve could be freely mobilized
within this area. No attempt was made to explore the nerve proximal to the
greater sciatic notch. Abnormal somatosensory evoked potential or
electromyographic responses prompted a brief halt in the dissection, with
reassessment of limb positioning and extension of the hip and flexion of the
knee as necessary. Dissection resumed when somatosensory evoked potential and
electromyographic activity returned to normal. Acetabular open reduction and
internal fixation or total hip arthroplasty was then performed.
Postoperatively, the patients walked with toe-touch weight-bearing for
three months. Prophylaxis against heterotopic ossification included
indomethacin alone or in combination with irradiation.
Sensory symptoms included radicular pain or paresthesias (seven patients)
and decreased sensation (three patients). All patients with sensory symptoms
obtained some degree of relief following sciatic nerve release
(Table I). Of the seven
patients with radicular pain or paresthesias, four had complete relief of
symptoms and the remainder had partial relief. Of the three patients with
diminished sensation, one had complete improvement and two had partial
improvement. Motor symptoms included weakness without a footdrop (two
patients) and a footdrop (five patients). None of the patients with motor
symptoms demonstrated complete resolution of those symptoms following
decompression (Table I). Both
of those with motor weakness and no footdrop had partial improvement in motor
function. Three of the five patients with a footdrop demonstrated no
improvement in motor function, and the remaining two had only partial
improvement. No patient had worse neurologic function after the nerve
decompression.
Sciatic nerve entrapment was observed intraoperatively in all patients.
Sites of nerve entrapment included the obturator and piriformis tendons (one
patient), scar tissue over the quadratus femoris muscle (one patient),
hemorrhagic tissue over the quadratus femoris muscle (one patient),
heterotopic bone and scar tissue at the acetabular fracture site (two
patients), heterotopic bone under the abductors (one patient), scar tissue at
the level of the lesser trochanter (one patient), and global scar tissue from
the greater sciatic notch to the ischium (three patients).
Preoperatively, hip flexion averaged 82° (range, 60° to 90°);
internal rotation, 3° (range, 0° to 10°); external rotation,
9° (range, 0° to 20°); abduction, 21° (range, 10° to
35°); and adduction, 13° (range, 5° to 20°). Postoperatively,
hip flexion averaged 98° (range, 90° to 120°); internal rotation,
11° (range, 10° to 30°); external rotation, 25° (range,
10° to 40°); abduction, 32° (range, 20° to 40°); and
adduction, 20° (range, 10° to 30°). One patient, a
twenty-one-year-old woman (Case 5; see Appendix) who had had a preoperative
sciatic neuropathy, underwent a revision total hip arthroplasty, because of
aseptic loosening, thirty-nine months after a primary total hip arthroplasty.
No further release of the sciatic nerve was performed at the time of the
revision arthroplasty. There was one deep venous thrombosis, which was treated
with long-term Coumadin (warfarin) therapy.
All patients were in general satisfied with the result of the procedure and
stated that they would undergo such surgery again under similar circumstances.
However, nine of the ten patients in our series underwent procedures in
addition to the sciatic nerve release, including open reduction and internal
fixation of the acetabulum and total hip arthroplasty, so it is difficult to
assess how much of this patient satisfaction was related to the nerve release
and sensory improvement and how much was related to improved mobility and
function after successful hip reconstruction.
There are only a few reports in the literature describing sciatic
neuropathy following severe acetabular trauma. In these reports, the
neuropathy presented in a delayed fashion, concurrent with the development of
heterotopic bone around the sciatic
nerve10,28,29.
Kleiman et al. reported a case in which sciatic nerve pain and weakness of
ankle dorsiflexion developed 4.5 months after open reduction and internal
fixation of a posterior fracture-dislocation of the
hip28. Sciatic
neurolysis with excision of heterotopic bone resulted in normal sensation but
no improvement in motor
function28. Thakkar
and Porter reported on a patient in whom pain and paresthesias along the
medial side of the leg and a footdrop developed after a fall on the buttock
three years after open reduction of a posterior hip
dislocation10.
Surgical exploration revealed heterotopic bone encasing the sciatic nerve;
surgical release of the nerve decreased sensory symptoms, but the footdrop
remained unchanged at the time of follow-up, two years postoperatively.
Hirasawa et al. reported a case in which sciatic neuropathy with paresthesias
and motor loss developed progressively over four months following open
reduction of a posterior hip
dislocation29. At
that point, sciatic nerve release was performed to free the nerve from
encasing heterotopic bone. Sensory function was almost completely restored and
motor function improved to a grade of 4 (of 5) at fifteen months after the
release. Taken together, these case reports seem to suggest that, at least in
cases of chronic nerve entrapment such as heterotopic bone encasement, lost
motor function is less likely to be recovered fully following sciatic nerve
decompression, which is consistent with our observations.
Surgical releases of the sciatic nerve have also been reported for
treatment of complications related to implants following total hip
arthroplasty8,9,23-25.
Uchio et al. reported a case of bilateral sciatic neuropathy occurring four
and six years following bilateral cementless total hip
arthroplasty23. A
hypertrophic posterior aspect of the hip capsule and a tense piriformis muscle
were found intraoperatively. The neuropathy resolved after sectioning of each
piriformis muscle and release of both sciatic nerves. Stiehl and Stewart
reported a case of delayed sciatic neuropathy after loosening of a pelvic
plate following complex acetabular reconstruction in hip
arthroplasty25.
Progressive neurologic signs of sciatic nerve compression developed six months
following reconstruction of a pelvic discontinuity. Sciatic nerve exploration
at one year identified a screw impinging on the nerve. The symptoms decreased
substantially following hardware removal and sciatic nerve release. Isiklar et
al. reported a case of delayed sciatic neuropathy resulting from intrapelvic
migration of an acetabular
cup9. This patient
had undergone a laminectomy, without relief of the symptoms, before the cup
migration was noted to be the problem. Removal of the protruding cup and
cement and acetabular revision resulted in complete resolution of the sciatic
neuropathy. Intraoperatively, the nerve was noted to be flattened at the
greater sciatic notch.
The question arises of whether surgical release of the sciatic nerve from
scar tissue and heterotopic bone improves neurologic outcomes compared with
the natural course of this disorder. Reports on the natural history of
posttraumatic or postoperative sciatic nerve palsies have provided conflicting
results. Letournel and Judet reported on thirty-four sciatic nerve injuries
that had occurred after surgical treatment of 569 acetabular fractures (a rate
of 6.0%)19. The
sciatic nerve injuries were noted immediately postoperatively, but it was
unclear if some of the deficits simply had not been detected preoperatively.
Eighteen of these palsies involved the peroneal division. One was a complete
lesion secondary to iatrogenic intraoperative nerve transection, and the
remainder were patchy lesions or pure sensory lesions. Nine palsies resolved
fully, and twelve decreased substantially. Two-thirds of the patients had no
sequelae. The recovery period extended up to three years.
Other surgeons have also reported favorable natural history. Epstein noted
that 60% of thirty-eight sciatic nerve injuries associated with posterior
fracture-dislocation of the hip resolved fully within three years after the
injury30. Schmeling
et al. observed that 100% of severe postoperative sciatic nerve palsies
involving the peroneal division resolved
fully31. Similarly,
Tile noted that 75% of posttraumatic sciatic nerve injuries and 100% of
postoperative sciatic nerve injuries resolved partially or
fully32.
Fassler et al. reported on fourteen patients with a displaced acetabular
fracture and a sciatic nerve
injury1. Eleven
injuries were posttraumatic, and three were iatrogenic. The authors classified
the injuries as mild (grade-3 or 4 [of 5] motor weakness or predominantly
sensory abnormalities) or severe (grade-0, 1, or 2 motor weakness with a
marked decrease or absence of sensation). They also divided injuries according
to whether there was involvement of the peroneal or tibial division. They
observed that patients with a mild peroneal nerve, mild tibial nerve, or
severe tibial nerve injury had substantial recovery at two years. When the
peroneal injury was severe, however, recovery was poor; only three of ten
patients with peroneal nerve injury had a satisfactory result, and one of
these patients was seventeen years old. There were seven footdrops, five of
which did not resolve.
Taken together, the conflicting results from the above studies suggest that
there are several confounding factors, including the anatomic location of the
lesion (peroneal or tibial division), severity of the trauma to the nerve
(neurapraxia, axonotmesis, or neurotmesis), impairment of sensory or motor
function, timing (posttraumatic or iatrogenic), chronicity of the lesion, and
patient age, that determine nerve recovery.
Our study had several limitations. It was a retrospective analysis of a
small number of symptomatic patients. There was no control group (i.e., no
similar cohort treated without nerve release). Thus, it is unclear if the
surgical release improved the neurologic outcomes of these patients compared
with the natural history of posttraumatic or postoperative sciatic nerve
palsies. While our findings suggest that motor function is less likely than
sensory function to return after nerve release, the average duration of
follow-up in our series was less than three years. As the peroneal division of
the sciatic nerve has been reported to exhibit recovery for up to three years
after injury19, it
is possible that some of the footdrops in our series will yet improve.
Certainly, a larger randomized study categorizing patients on the basis of
potential confounding factors such as age, location of the lesion, nature of
the nerve injury, impairment of sensory or motor function, degree of
involvement, and timing of decompression will allow a more objective
assessment of the benefits of surgical release.
A potential diagnostic problem encountered during the examination of a
patient with an acetabular fracture and a sciatic nerve injury is the
identification of the contribution of preexisting lumbosacral degenerative
disease or pelvic or spine trauma to the neurologic findings. While there are
reports in the literature of inappropriate lumbar decompression for
extraspinal sciatic nerve
entrapment8,9,
the reverse—sciatic nerve decompression in the pelvis when the
neurologic symptoms are caused predominantly by nerve root compression in the
lumbar spine—may also occur. While a careful physical examination, with
assessment for localized tenderness, step-off, and myelopathy, was performed
on the patients in this series, the lumbar spine was not routinely imaged with
computed tomography, magnetic resonance imaging, or computed
tomography-myelography to objectively quantify lumbar degenerative disease.
However, the absence of substantial spinal trauma or pelvic ring disruption in
our patients at the time of the acetabular fracture and the temporal
relationship between the onset of sciatic nerve-related symptoms and the
acetabular trauma or reconstructive surgery suggest that the etiology of the
neurologic symptoms was more likely related to the sciatic nerve injury than
to lumbosacral nerve-root injury. Nevertheless, prospective studies in which
cases of spinal trauma and spinal stenosis either are excluded or are
randomized as confounding variables will allow a more scientific evaluation of
the role of surgical release on nerve recovery.
Our experience indicates that careful release of the sciatic nerve from the
greater sciatic notch to below the insertion of the gluteus maximus tendon
during reconstructive acetabular surgery results in a marked decrease in
preoperative sensory sciatic neuropathic symptoms, including radicular pain,
paresthesias, and diminished sensation.
We did not explore the sciatic nerve proximal to the greater sciatic notch
because of the difficulty with accessing the intrapelvic portion of the nerve.
Compression of the sciatic nerve within the pelvis may compromise the result
achieved by decompression of the extrapelvic portion of the nerve. Osteotomy
of the greater sciatic notch can improve access to the nerve, but it is a
dangerous procedure and can result in further sciatic nerve or superior
gluteal vessel trauma. While the majority of patients with motor symptoms
demonstrated improvement, footdrop was less likely to completely resolve after
nerve release. None of the patients in our series had worse neurologic
function following nerve decompression. However, rigorous determination of
whether sciatic nerve release improves neurologic outcome compared with the
natural history of sciatic nerve injuries will require prospective,
randomized, controlled studies.
A table showing clinical details on all study patients is available with
the electronic versions of this article, on our web site at
(go to
the article citation and click on "Supplementary Material") and on
our quarterly CD-ROM (call our subscription department, at 781-449-9780, to
order the CD-ROM). ?
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